ANovelIndexforPromptPredictionofSeverityinPatientswith ...femalepatientshasbeenreportedtobe18.7%,withthemost commonpredisposingcausesknowntobecoronaryartery disease,hypertension,andleftventricularhypertrophy[7]

Research ArticleA Novel Index for Prompt Prediction of Severity in Patients withUnstable Angina Pectoris

Mustafa Bolatkale1 and Ahmet Cagdas Acara 2

1Medipol University Hospital, Department of Emergency Medicine, Istanbul, Turkey2Bozyaka Research and Training Hospital, Department of Emergency Medicine, Izmir, Turkey

Correspondence should be addressed to Ahmet Cagdas Acara; [email protected]

Received 23 July 2019; Revised 26 November 2019; Accepted 6 December 2019; Published 3 January 2020

Academic Editor: Robert Derlet

Copyright © 2020 Mustafa Bolatkale and Ahmet Cagdas Acara. *is is an open access article distributed under the CreativeCommons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided theoriginal work is properly cited.

Objectives. Rapid risk stratification by emergency department (ED) physicians to evaluate patients with chest pain for predictingthe short-term occurrence of major adverse cardiac event (MACE) is crucial.*e aim of this study was to investigate the predictivevalue of platelet-lymphocyte ratio (PLR) levels and compare with the modified heart score (m-HS) and stress testing to predict theseverity of high-risk patients with unstable angina pectoris (UAP) in the ED. Methods. *is study is prospective which included316 patients with UAP and 316 control healthy subjects. *e study took place from 01 April 2016, until 01 April 2017, in MedipolUniversity. Result. *e mean PLR levels in the UAP group were higher than those in the control group (p< 0.001). *e mean PLRof the m-HS ≥4 group was higher than that in the m-HS ≤3 group (p< 0.001). *e mean levels of PLR in the subgroups based onthe stress testing positivity were higher than those in the stress testing negative subgroup (p< 0.001). PLR levels were positivelycorrelated with the m-HS, stress testing, and treatment decision in this study (r� 0.559; p< 0.001; r� 0.582; p< 0.001; r� 0.789;p< 0.001, respectively). Conclusion. A positive correlation was determined with an increase in m-HS, treatment decision, andpositive exercise testing as the PLR levels increased, indicating the severity of high risk of UAP in the ED.

1. Introduction

Acute coronary syndrome (ACS) is the leading cause ofdeath worldwide. ACS covers a wide spectrum of clinicalconditions, ranging from unstable angina pectoris (UAP) tonon-ST elevation myocardial infarction (N-STEMI) or STelevation myocardial infarction (STEMI). UAP andNSTEMI are closely related conditions, with similar path-ophysiological origins and clinical presentations, but theydiffer in severity. In a patient experiencing UAP, no bio-marker can be detected in the bloodstream hours after theinitial onset of ischemic chest pain [1]. Although only whiteclots are found in patients with UAP/NSTEMI, red clotsform in patients with STEMI [1]. UAP is considered underthe umbrella term of ACS, in which patients are admittedwith acute chest pain or shortness of breath, with neither STelevation nor abnormal cardiac enzymes [2]. UAP ischaracterized by

female patients has been reported to be 18.7%, with the mostcommon predisposing causes known to be coronary arterydisease, hypertension, and left ventricular hypertrophy [7].

A significant proportion of patients with chest painundergo advanced medical evaluation during visits, result-ing in longer and more costly ED stays. Many patientspresenting with chest pain are currently hospitalized andextensively evaluated with noninvasive stress testing orimaging or with invasive coronary angiography (CAG) [2].*e gold standard diagnostic test for ACS is CAG, but thiscannot be applied to all cases of chest pain due to UAP in theED [4].

*ere are many risk stratification scores for ACS, butwith the exception of the modified-heart score (m-HS),scoring systems are time-consuming and can delay treat-ment in patients with ACS caused by myocardial damagedue to low ejection fraction. M-HS is a rapid risk stratifi-cation tool, designed by ED physicians to evaluate patientswith chest pain according to their short-term risk of majoradverse cardiac event (MACE, defined as acute myocardialinfarction (AMI), need for percutaneous coronary inter-vention (PCI) or coronary artery bypass graft surgery(CABG), and death within 6 weeks) to help identify low-riskpatients, suitable for earlier ED discharge within 30 days ofindex ED visit [8, 9]. However, the original HS included cTnlevels in the score in a way that allowed a patient with anelevated cTn to be considered low-risk [8]. Generally, high-risk patients are admitted to the cardiology or medical wardsand those at low risk are managed in an observation unit orsent home.

In the pathophysiology of ACS, inflammatory mediatorsand endothelial dysfunction play a pivotal role in the cor-onary inflammation found during UAP [10]. Platelets play akey role in the pathophysiology of ACS. Higher levels ofinflammatory markers are associated with the severity ofcoronary artery disease (CAD) and worse cardiovascularoutcome [11]. *e platelet-lymphocyte ratio (PLR), which iscalculated by the division of absolute platelet count byabsolute lymphocyte count, has been stated to be a newindicator of inflammatory response. Inflammation leadingto ACS has encouraged research into the clinical usage ofnew inflammatory biomarkers [9]. *e PLR has beenclaimed to be a marker to help identify thrombotic activityand inflammation in cardiac diseases [12].

Early diagnosis and the initiation of appropriate treat-ment within 24 hours are essential to reduce UAP-relatedmortality and morbidity [13]. If patients at high risk of UAPcould be recognized early in the diagnostic process, mor-tality, morbidity, and negative effects of delayed treatmentcould be potentially reduced and a good outcome could beprovided with cost-effective treatments [10].*erefore, thereis still a need for a sensitive, specific marker for the pre-diction of severity in patients with UAP.

Recent studies have shown that PLR, which is evaluatedas a prognostic marker of ACS, may also be increased inpatients with N-STEMI and STEMI [14, 15]. Previousstudies have revealed that PLR levels are significantly in-creased in MI, stroke, and subsequent heart failure [16].However, there are no studies regarding PLR levels in

patients with UAP and no studies which have examined PLRlevels compared with m-HS and stress testing to predict theseverity and make the treatment decision in patients withUAP.

*e aim of the present study was to compare PLR levelswithm-HS and stress testing in the prediction of severity andtreatment decision in patients with UAP.

2. Methods

Approval for this prospective study was granted by theMedipol University Clinical Research Ethics Committee(decision no: 11.03.2016/E.3931-145). *is prospective studywas conducted in the Medipol University Hospital AdultED. *e study took place from 01 April 2016, until 01 April2017. All patients provided signed informed consent. *estudy was performed in accordance with the Declaration ofHelsinki.

2.1. Study and Control Groups. Our study group was com-prised of adult patients with a diagnosis of UAP diagnosed inthe ED. *e control group was comprised of healthy adultswith no acute or chronic disease. Patients were excluded ifthey had a previously known disease which would explainthe chest pain other than angina or if they did not agree toparticipate in the study. All patients in both groups were ≥18years old. *e groups were classified as “UAP” and “Con-trol.” Gender, age, and PLR levels were recorded for bothgroups, and the latter was examined in the UAP group:blood urea nitrogen (BUN), creatinine, hemograms, CK-MB, 0 and 3-hour cTnI, m-HS, stress testing results, andtreatment decision. *e patients with UAP were separatedinto 3 subgroups, based on low (≤3) and high (≥4) m-HS [4],positive and negative stress testing, and the treatment de-cision of CAG (only conventional medical treatment), PCI,and CABG.

2.2. Biochemical Analysis. All blood samples were takenfrom the brachial veins. Creatinine and BUN were measured(Cobas 6000 auto analyzer, Roche, Tokyo, Japan). Bloodsamples for hemograms were collected in 2ml ethyl-enediaminetetraacetic acid (EDTA) tubes and analyzedusing an automated hematology analyzer (XT-2000I; Symex,Osaka, Japan). *e PLR levels were calculated as the ratio ofplatelet count to lymphocyte count. Blood samples werecentrifuged within 30 minutes and CK-MB, and 0- and 3-hour cTnI were determined using an AQT90 FLEX analyzerdevice (Radiometer, Copenhagen, Denmark) with the im-munoassay method. Cutoff values for CK-MB and cTnI were7.2 μg/L and 0.023 μg/L, respectively.

2.3. m-HS and Stress Testing. *e m-HS was prospectivelyapplied to the population in the ED. *e acronym m-HS isan abbreviation of the four parameters evaluated [5]: history(highly suspicious—2 points; moderately suspicious—1point; slightly suspicious—0 points), ECG (significant ST-depression—2 points; nonspecific repolarization

2 Emergency Medicine International

disturbance—1 point; normal—0 points), age (≥65 years—2points; 45–65 years—1 point; ≤45 years—0 points), riskfactors for coronary heart disease (≥3 risk factors—2 points;1 or 2 risk factors—1 point; no risk factors—0 points). *eidentified risk factors for coronary heart disease includeprior acute MI, percutaneous coronary intervention orcoronary artery bypass grafting surgery, hypertension, di-abetes mellitus, smoking history, hyperlipidemia, and familyhistory.

According to the total score applied, patients with UAPwere separated as m-HS ≤3 low risk and m-HS ≥4 high riskof a MACE, within 6 weeks after presentation at the ED [8].Lower scores (m-HS≤ 3) led to a recommendation of earlydischarge, and high scores (HS≥ 4) suggested clinical ob-servation or performance of noninvasive investigations andadmission for more invasive strategies [8]. Stress testing wasapplied to patients with UAP with m-HS ≤3. *e stresstesting was modified according to the Bruce protocol [17].

2.4. Statistical Analysis. Statistical analyses of the data ob-tained in the study were made using SPSS 25.0 software(SPSS Inc., Chicago, IL, USA). Variables were stated asmean± standard deviation or median with interquartilerange. Student’s t test was used to compare mean values, andthe Mann–Whitney U test was used to compare medianvalues. Frequencies were compared with the chi-squared andFisher’s exact tests. Spearman’s correlation tests were ap-plied for correlation analyses. *e median and mean PLRvalues were calculated. To determine a cutoff value of PLRlevel for UAP, receiver operating characteristic (ROC)analysis was performed in sensitivity and specificity calcu-lations. Receiver-operating characteristic analyses were usedto detect the cutoff value of PLR in the prediction of low tohigh m-HS. *e PLR levels were compared between thesubgroups based on the m- HS, stress testing, and treatmentsusing one-way analysis of variance (ANOVA) testing withleast significant difference (LSD) post hoc analysis. A valueof p< 0.05 was considered statistically significant.

3. Results

During the study period, a total of 14,876 patients wereadmitted to the ED. After application of the exclusion cri-teria, 316 patients in the ED with UAP were included as thestudy population. *e study included 316 patients admittedwith UAP and 316 control healthy subjects. *e mean agewas 64.68± 10.67 years in the UAP group and 63.89± 10.42years in the control group (p� 0.346). *e UAP group wascomprised of 112 (35%) females and 204 (65%) males, andthe control group was comprised of 118 (37%) females and198 (63%) males (p � 0.621). *e mean platelet levels of theUAP group (241.43± 55.48 103/μL) were higher than thoseof the control group (221.58± 56.78 103/μL) (p< 0.001). *emean lymphocyte levels of the UAP group (2.25± 0.87 103/μL) were higher than those of the control group (2.12± 0.51103/μL) (p: 0.025).

*e mean lymphocyte levels of the UAP group were2.25± 0.87 103/μL. In the control group, the mean platelet

levels were 221.58± 56.78 103/μL and lymphocyte levels were2.12± 0.51 103/μL. *e mean PLR levels of the UAP group(130.09± 48.52) were higher than those of the control group(99.01± 21.51) (p< 0.001).

*e area under the ROC curve for PLR level was 0.713(95% confidence interval [CI], 0.672–0.753), and the PLRlevel had sensitivity of 58.2% and specificity of 80.4% at117.99. When the m-HS of the 316 patients in the study wereexamined, 154 patients were evaluated with m-HS of ≥4 and162 patients with m-HS ≤3. *e mean PLR of the m-HS ≥4group (n: 154) was higher than that of the m-HS≤ 3group (n: 162) (152.76± 52.25 vs. 108.54± 32.46; p< 0.001)(Figures 1 and 2).

*e area under the ROC curve for PLR level in the UAPsubgroups based on m-HS, between m-HS ≤3 (low) andm-HS of ≥4 (high), was 0.770 (95% confidence interval (CI),0.720–0.821). *e PLR level had sensitivity of 71.4% andspecificity of 74.1% at 125.40.

Exercise testing was applied to 162 patients with m-HS≤3. Of these, 53 had positive exercise testing output, 30patients underwent PCI, 4 patients underwent CABG, and19 patients had taken only conventional medical treatment.*e mean levels of PLR in the subgroups based on the stresstesting positivity (135.55± 30.08) were higher than in thestress testing negative subgroup (95.40± 25.57) (p< 0.001)(Figure 3).*emean levels of PLR in the subgroups based onthe stress testing positivity with significant CAD (n: 34;151.47± 23.87) were higher than those in the stress testingpositivity without significant CAD subgroup (n: 19;107.06± 15.27) (p< 0.001).

PLR levels were positively correlated with stress testingin this study (r� 0.582; p< 0.001, Figure 4).

*e area under the ROC curve for PLR level in the UAPsubgroups based on exercise testing to differentiate betweenstress testing abnormal and normal was 0.843 (95% confi-dence interval (CI), 0.782–0.903), and the PLR level wasdetermined with sensitivity of 84.9% and specificity of 73.4%at 112.02.

*e PLR levels were statistically significantly different inthe subgroups based on treatment decision (p< 0.001,ANOVA test). *e mean PLR level was 103.95± 12.36 in theCAG subgroup (n: 48), 146.37± 26.69 in the PCI subgroup(n: 135), and 248.34± 41.00 in the CABG subgroup (n: 24)(p< 0.001). A positive correlation was determined betweenPLR levels and treatment decision in this study (r� 0.789;p< 0.001, Figure 5).

4. Discussion

In this study, PLR levels were compared with m-HS andstress testing in the prediction of low-high risk and treat-ment decision in patients with UAP in the ED. A positivecorrelation was determined with an increase in m-HS andpositive exercise testing as the PLR levels increased, indi-cating the severity of high risk of UAP in the ED. *ecorrelation between PLR levels and the treatment decisionprovides early information about patients admitted to theED in respect of prognosis, and thus the decision oftreatment for chest pain due to UAP can be guided. To the

Emergency Medicine International 3

best of our knowledge, this is the �rst study to have dem-onstrated an association of PLR levels with them-HS and theseverity of coronary atherosclerosis in patients with UAP.According to the current study �ndings, higher PLR valueson admission were signi�cantly associated with high m-HSin patients with UAP.

Atherosclerosis is a complex and multifactorial in-ammatory disease characterized by low-grade arterial in-ammatory lesions that can develop through CADprogression, and inammatory markers can be shown incirculation [18–20]. Inammation plays a key role in thedevelopment, progression, and complications of athero-sclerosis. Previous studies have demonstrated that higherplatelet and lower lymphocyte counts are associated withMACE and poor clinical outcomes in various cardiovasculardiseases [17, 21]. Platelets play a major role in the athero-thrombotic process and pathogenesis of AMI, and an ele-vated platelet count is related to increased infarct size as wellas short- and long-term worse prognosis in patients withAMI [22]. e CADILLAC study showed that the level of

Negative (n: 109)

p < 0.001

Stress testingPositive (n: 53)

200.00

175.00

150.00

125.00

100.00

75.00

Plat

elet

/lym

phoc

yte r

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Figure 3: Distribution of PLR levels for each subgroup accordingto exercise testing (PLR: platelet-lymphocyte ratio).

200.00

175.00

150.00

125.00

100.00

75.00

Stress testing

r = 0.582; p < 0.001

Negative Positive

Plat

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Figure 4: Correlation between PLR levels and stress testing (PLR:platelet-lymphocyte ratio).

250.00

200.00

150.00

100.00

300.00

50.00

CAG PCI

r = 0.789; p < 0.001

CABG

Plat

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Figure 5: Correlation between PLR levels and treatment decision(PLR: platelet-lymphocyte ratio; CAG: coronary angiography; PCI:percutaneous coronary intervention; CABG: coronary artery by-pass graft).

p < 0.001

m-HS ≤ 3 (n: 162) m-HS ≥ 4 (n: 154)

57 294 215313 76

155234

136

50.00

100.00

150.00

200.00

250.00

300.00

Plat

elet

/lym

phoc

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Figure 1: Distribution of PLR levels for m-HS ≤3 and m-HS ≥4subgroups (PLR: platelet-lymphocyte ratio; m-HS: modi�ed-heartscore). PLR levels were determined to be positively correlated withm-HS (r� 0.559; p< 0.001, Spearman’s).

2 4Modified-heart score

r = 0.559; p < 0.001

6 8 50.00

100.00

150.00

200.00

250.00

300.00

Plat

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Figure 2: Correlation between PLR levels andm-HS (PLR: platelet-lymphocyte ratio; m-HS: modi�ed-heart score).


platelets (which does not affect the effectiveness of percu-taneous interventions) is significantly correlated with theincidence of restenosis and stent thrombosis [16].

Low lymphocyte count is related with increased in-flammation, and a low lymphocyte count is a worse prog-nostic marker in patients with CAD [22]. Lymphocytes are amajor part of chronic inflammation in the atheroscleroticprocess and infiltrate the ischemic myocardium during AMI[22]. A lower lymphocyte count due to increased cortisol as aresponse to stress has been associated with high mortalityrates in AMI [22]. It has been proposed that, in response tophysiological stress during myocardial ischemia or infarc-tion, there is a release of cortisol and catecholamine, re-distribution of lymphocytes to lymphatic organs, andapoptosis, which lead to lymphopenia [21]. A high level ofphysiological stress means high levels of cortisol and cate-cholamine, which can be translated into a lower lymphocytecount.

PLR is calculated from systemic inflammatory markersas a predictor of poor cardiovascular outcomes [11]. Recentstudies have demonstrated that the PLR is associated withMACE and that it is an independent marker of mortality insome oncological and cardiac diseases [12, 23, 24]. In arecent study, a high PLR was found to be correlated with therecurrence of MI, stroke, and subsequent heart failure [16].However, its relationship with UAP severity is not yetknown. In the present study, high PLR levels may be anindication of increased inflammatory response, which isrelated to the extent of inflammation, atherosclerosis, andthromboembolic states. In another recent study, the PLRlevel was reported to be independently associated with theGENSINI score together with white blood cell (WBC) count,age, and low high-density lipoprotein (HDL) in multivariateanalysis [11].

*e m-HS includes elements of the history, ECG, age,and risk factors [8]. However, in the original HS, cTn levelswere considered in a way that allowed a patient with anelevated cTn to be evaluated as low-risk [8]. In a previousstudy, it was suggested that when normal serial cTn valuesare combined with the HS, a very low-risk patient pop-ulation can be identified, which could be discharged fromthe ED without further testing [8]. Low-risk patients (a scoreof ≤3) have been reported to have a low (1.7%) MACE rate[9]. *e majority of physicians deem a miss rate of 36 hoursafter presentation) in 3,031 high-risk patients with UAP/NSTEMI [1]. With the exception of high-risk patients with aGrace (Global Registry of Acute Coronary Events) risk score>140, the early invasive strategy was not seen to be superiorto the delayed invasive strategy in reducing the primary endpoint of death, MI, or stroke at 6 months [1].

Antiplatelet and anticoagulant medication given to pa-tients during ACS and PCI have significantly reduced thereinfarction and lowered the mortality rates [27]. *ese drugsare administered in catheter laboratories for emergency PCI,but in cases not treated due to operation failure or inap-propriate anatomy and in those for whom an urgent CABGdecision is made before the PCI procedure, these drugs cansignificantly increase the bleeding and hemorrhagic mortality,with the exception of cangrelor [28, 29]. Although urgentCABG surgery is recommended, the operation of these pa-tients is delayed in many centers, and because of prolongedwaiting time for CABG, the mortality rates increased in pa-tients with CAD [30]. *e results of the current study dem-onstrating the correlation of high m-HS and positive stresstesting with high PLR levels have shown that there is a highlikelihood that in cases of CAD referred for CA are preferentialcandidates for interventional therapies such as PCI andCABG.*e bleeding andmortality ratesmay be reduced in associationwith antiplatelet and anticoagulant doses, which can beestablished through early consultation with cardiovascularsurgeons before applying CAG.

Early diagnosis and the initiation of appropriate treat-ment within 24 hours are essential to reduce UAP-relatedmortality and morbidity rates [13]. *is early prediction ofseverity and ischemia using a biomarker is important as itmay improve the risk stratification of UAP patients, guidetreatment decisions, and preserve patients from MACE and


the risk of sudden cardiac death. Furthermore, this study hasdemonstrated that an increased PLR level on admission is anindependent predictor of high risk for UAP. *e results ofthe study have shown that PLR indices are sufficient to showhigh risk in patients with UAP and have a strong positivecorrelation to m-HS ≥4. *us, the study hypothesis con-firmed that PLR may be useful as a predictive biomarker forUAP because it can indicate the severity of CAD in patientswith UAP. If these results are confirmed by further studies,the use of PLR may improve current predictive, prognosticstrategies, and guide treatment decisions in patients withUAP in the ED.

5. Conclusion

In the present study, blood PLR levels were observed to besignificantly increased in adult patients with UAP comparedto healthy control subjects, and a strong positive correlationwas determined between PLR and m-HS scores. Higher PLRmay indicate an increased inflammatory response, which isrelated to the severity of coronary atherosclerosis in patientswith UAP and this could therefore be a part of cardiovas-cular evaluation in the ED before further examination andtreatment decision. PLR appears to be a cost-effective andpractical tool predicting the severity of coronary athero-sclerosis in patients with UAP. A positive correlation wasdetermined with an increase in m-HS, treatment decision,and positive exercise testing as the PLR levels increased,indicating the severity of high risk of UAP in the ED.

6. Study Limitations

PLR may be affected by several pathological variables.However, it was not possible in this study to control all thevariables that could influence PLR levels. *ere was nocomparison of other inflammatorymarkers in the predictionof severity of UAP.*e contact time to hospital was acceptedas the initial hour for the purposes of this study. *e periodwhich started after the collection of the first blood sampleswas not standardized in every patient, and the number ofsubjects included in the study was limited.

Data Availability

*e data used to support the findings of this study areavailable from the corresponding author upon request.

Conflicts of Interest

*e authors declare that there are no potential conflicts ofinterest regarding the publication of this article.

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[30] V. B. P. Da Fonseca, A. De Lorenzo, B. R. Tura, F. J. M. Pittella,and A. S. C. da Rocha, “Mortality andmorbidity of patients onthe waiting list for coronary artery bypass graft surgery,”Interactive Cardiovascular and9oracic Surgery, vol. 26, no. 1,pp. 34–40, 2018.


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